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Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease. PD invariably manifests with motor symptoms related to the dopaminergic cell loss in the substantia nigra pars compacta. In the early stages, patients usually experience some bradykinesia, rigidity and, often, some tremor. The symptoms are typically asymmetric at onset. The age of presentation varies considerably, with young-onset PD arbitrarily being defined as onset before 50 years of age. The incidence and prevalence of PD rise with increasing age; the peak incidence is in the early 60s. Dopaminergic cell loss continues with the progression of the disease. Various imaging markers have suggested a rate of cell loss between 6 and 12% per annum in the early stages of PD. However, the rate of cell loss may vary, probably being greatest in the earlier phases of the disease. The preclinical latent period, during which cells are dying but clinical features are not apparent, has been variously estimated at between 5 and 10 years. Again, however, this period varies, probably according to etiology.
Although the early symptomatic features of PD are related to dopaminergic cell loss, in later stages of the disease the effect of neuronal loss in other neurotransmitter systems becomes apparent. These nonmotor features include autonomic dysfunction and cognitive abnormalities. Although symptomatic treatments are available to reverse the dopaminergic features of PD, no successful treatments are yet available for the nondopaminergic features. These inevitably become the most disabling element of PD, and the cognitive dysfunction, in particular, is often a reason for institutionalization.
Various treatments are now available for the symptomatic management of PD. These are predominantly related to the dopaminergic system and include l-dopa, dopamine agonists (DAs), and monoamine oxidase-B inhibitors (MAOIs). Other drugs, such as anticholinergics and amantadine, may have a beneficial effect on motor …
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